Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and morphological analysis is reported of the changes evolving in 12 cases of mesangial proliferative glomerulonephritis based on repeated biopsies carried out at intervals from 1 to 7 years. Clinical findings at the time of the first biopsy included in 2 cases nephrotic syndrome, and in the remaining cases proteinuria ranging from 0.3 to 2/1000. In all cases erythrocytes in urine were present ranging from 4-6 to 50-100 erythrocytes per field of vision. Hypertension was found in 4 cases, and increased serum creatinine level in 1 patient. At the time of repeated biopsy in 11 cases clinical evidence of improvement was noted with decreased proteinuria anderythrocytes in urine. In 1 case worsening was found and several months later signs of renal failure developed which led to death. The morphological examinations demonstrated in the first biopsies mesangial proliferative glomerulonephritis. In second biopsies these findings were confirmed. In 1 case with unfavourable outcome the changes became more pronounced, and in the remaining ones no significant differences were noted in relation to the first biopsy which evidenced lack of a close correlation between the clinical condition and the morphological state of the kidneys.
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PMID:[Evolution of morphological and clinical changes in mesangial proliferative glomerulonephritis]. 127

ACE inhibitors which till recently were used only in the treatment of cardiovascular diseases are becoming a perspective group of drugs also in the treatment of chronic nephropathies. It was revealed that they are effective in particular in the treatment of proteinuria of different etiology and have also a marked renoprotective effect and are therefore recommended to slow down the progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard the progression of chronic glomerulonephritis and diabetic nephropathy. It may be excepted that their therapeutic application will in the near future be extended also to clinical nephrology.
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PMID:[ACE inhibitors--a prospective new group of drugs for the treatment of kidney diseases]. 129 14

Clinicomorphological analysis has been performed in Schoenlein-Henoch nephropathy. Various clinical symptoms are accompanied by morphological changes of variable type and severity. Electron microscopy is a major tool for evaluating these changes. It relatively frequently modifies the diagnosis made by light microscopy. It mainly concerns class I and VI changes (according to a grading system of the International Study Group of Kidney Diseases in Childhood). It was shown that late prognosis was largely determined by the type and severity of morphological changes. Varying severity of changes in individual glomeruli in the same specimen requires in each case a comparison of results obtained by electron microscopy with those obtained by light microscopy in semithin sections. In three children biopsy was repeated. Progression of morphological changes was found in one child. He developed renal failure. In one child morphological changes on first biopsy did not differ from those on second biopsy. Repeated biopsy was performed due to the presence of hypertension. In one child with persistent proteinuria repeated biopsy showed marked attenuation of morphological changes.
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PMID:The clinicomorphological correlations in Schoenlein-Henoch nephropathy in children. 129 73

Reflux nephropathy (RN), the main complication of the vesico-ureteral reflux (VUR), relatively frequent in adults, is often the consequence of recurrent urinary infections in the child, hood or during pregnancy. Unilateral RN has generally a benign course but the bilateral one, with important nephron destruction, leads to focal and segmental glomerulosclerosis, manifested by high levels of proteinuria. A certain degree of cicatrization and renal failure are followed by progressive impairment of the remaining renal function, even if VUR is cured. An early diagnosis, treatment of the acute bacterial infection, adequate ingestion of liquids, regulation of the intestinal transit and complete bladder voiding by miction, associated with hypotensive and antiinfectious drug therapy lead to VUR disappearance in 80% of the cases, avoiding renal failure. Surgery is indicated only in the patients with severe reflux and with congenital or obstructive anomalies, as well as in the case of recurrent infection resistant to antibiotherapy.
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PMID:Reflux nephropathy in adults. 129 13

The human immunodeficiency virus (HIV) was recently suggested to be involved in generating kidney lesions in HIV-associated nephropathy (HIVN). The possibility that antiretroviral agents can slow down the usually explosive evolution of HIVN to end-stage renal failure (ESRF) has not been studied in many of the series of cases published. The present work is a retrospective analysis of 11 patients with histologically proven HIVN, 6 of whom were treated with zidovudine. Seven patients (group 1) either required dialysis at the outset, when HIVN was diagnosed, or progressed very fast to ESRF within 15-45 days. Two patients of this group were treated with zidovudine, but it had no effect on kidney function. In the remaining 4 patients (group 2), HIVN progressed more slowly than in group 1. All 4 patients were treated with zidovudine at an earlier stage of the disease than ESRF. Only 1 deteriorated to ESRF in 9 months. The 3 others, who did not have ESRF, were followed up for 13, 10 and 32 months, respectively. Although this is a preliminary study, its results do suggest that zidovudine can slow down the evolution of HIVN to ESRF. They highlight the need to screen HIV-positive patients regularly for proteinuria, in order to detect HIVN by renal biopsies at an early stage of renal lesion formation.
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PMID:Nephropathy associated with infection by human immunodeficiency virus: a report on 11 cases including 6 treated with zidovudine. 130 Apr 39

Patients with end-stage renal failure secondary to idiopathic nephrotic syndrome are at risk of initial disease recurrence after kidney transplantation (30%). Selective proteinuria can appear immediately after transplantation and focal glomerular sclerosis with graft loss can occur in 10% of patients with recurrence. Current immunosuppressive protocols do not seem to influence the recurrence rate in adult patients and the efficacy of therapeutic plasma exchanges remains controversial. We have previously demonstrated that plasma exchanges, proposed early before glomerular sclerosis, were able to significantly reduce proteinuria without affecting albuminemia or glomerular filtration. We report here on three patients who suffered immediate recurrence after transplantation and were treated with plasma immunoadsorption onto protein A column (Excorim, Lund); these patients had prior histories of steroid-resistant focal glomerular sclerosis. This procedure is more specific than plasma exchange in that it cleared the serum of immunoglobulins, significantly decreased proteinuria in only two cases (from 14 to 5 g/d and 2.5 to 0.8 g/d) and eliminated it in the third case (from 3 to 0.1 g/d). The modifications of proteinuria levels appeared as early as the second immunoadsorption sequence and returned to pre-immunoadsorption values within 2 to 8 weeks. These observations argue for the protein A binding of plasmatic factor(s) involved in idiopathic, nephrotic syndrome and allow us to progress to the characterization of this(ese) factor(s).
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PMID:Effects of plasma-protein A immunoadsorption on idiopathic nephrotic syndrome recurring after renal transplantation. 130 Aug 88

Several authors described a high incidence of proteinuria with frequent progression to nephrotic syndrome and/or renal failure in patients with HIV infection. Though renal histological changes were rather non-specific, the existence of a specific, HIV-associated glomerulopathy was postulated. We repeatedly investigated proteinuria and serum creatinine in 203 HIV-infected patients. One hundred and twenty-two patients (group 1) had early stages of the disease without opportunistic infections, 81 suffered from acute opportunistic infections (group 2). In patients with a positive qualitative test (Combistix), quantitative measurement (Biuret) for proteinuria was carried out; when proteinuria was greater than 0.5 g/24 h, SDS gel electrophoresis was performed. None of the patients of group 1 had a proteinuria greater than 0.5 g/24 h or an elevated serum creatinine. Eleven of 81 patients from group 2 had a proteinuria between 0.5 and 3 g/24 h; one further patient of group 2 developed a transient proteinuria of 7.7 g/24 h. Only three of the proteinuric patients showed a glomerular pattern in SDS gel electrophoresis, all three during acute CMV or EBV infections. Fourteen of 81 group 2 patients showed a transient elevation of serum creatinine (x +/- SD of the maximum serum creatinines: 225.3 +/- 163 mumol/l), most during pentamidine therapy for Pneumocystis carinii infection; one patient treated with high-dose acyclovir had to be temporarily dialysed. In the investigated 203 HIV patients no nephrotic syndrome and no sustained elevation of serum creatinine greater than 200 mumol/l was observed. All cases of proteinuria and elevation of serum creatinine were associated with severe opportunistic infections and the administration of potentially nephrotoxic antibiotics.
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PMID:Lack of clinical evidence for a specific HIV-associated glomerulopathy in 203 patients with HIV infection. 131 85

We have studied glomerular basal laminar thickness in biopsy material, using a simple technique involving 16 selected measurements per case. Twenty-nine biopsied cases of adult glomerular haematuria were examined together with 'diseased' controls represented by a variety of glomerulopathies including minimal-change disease and IgA nephropathy. 'Normal' control populations were provided by 13 patients with acute-onset renal failure of non-glomerular origin and nine patients undergoing nephrectomy. Analysis of groups determined by the presence or absence of haematuria, the degree of proteinuria and presence or absence of a diagnostically characteristic immunofluorescence pattern showed that the nine patients with haematuria and proteinuria of less than 200 mg/24 h represented a distinct subpopulation with a mean membrane thickness of 225 nm compared to the control mean of 343 nm (P less than 0.0001). All members of this subpopulation had mean values below an arbitrary cut-off value of 270 nm. Within other specific disease categories, sporadic cases had mean membrane thicknesses below this critical value, indicative of an overlap of pathologies. On short-term follow-up there is no evidence that the 'pure' thin-membrane population are subject to any deterioration in renal function. It is of further interest that eight of nine thin-membrane 'syndrome' cases were O Rh positive. This finding may provide a starting point for investigation of a specific genetic defect.
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PMID:Glomerular basement membrane thinning in adults: clinicopathological correlations of a new diagnostic approach. 131 88

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

Diagnostic criteria of analgesic nephropathy with well-defined sensitivity and specificity are not available. During a 2-year period all new patients (n = 273) starting renal replacement therapy in 13 Belgian dialysis units were investigated aiming to select diagnostic criteria of analgesic nephropathy with acceptable performance. Using several interview techniques, a history of analgesic abuse was found in 31% of the patients. Analgesic abusers presenting a clear non-analgesic-related renal diagnosis were excluded from analysis (n = 25). Comparing the remaining abusers (n = 60) and patients without a history of analgesic abuse (n = 188) it was found that renal imaging investigations (sonography plus tomography), showing a decrease in length combined with bumpy contours of both kidneys, presented a sensitivity of 90% and a specificity of 95%. The additional finding of signs of renal papillary necrosis resulted in an overall sensitivity of 72% and a specificity of 97%, giving a positive predictive value of 92%. Other signs frequently mentioned in the literature (hypertension, anaemia, sterile pyuria, bacteriuria, proteinuria) showed insufficient sensitivity and/or specificity to be of help for diagnosing analgesic nephropathy in end-stage renal failure (ESRF) patients starting renal replacement therapy.
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PMID:Diagnostic criteria of analgesic nephropathy in patients with end-stage renal failure: results of the Belgian study. 132 Feb 26


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